The discovery that memory, behavior, cognition, and thought processes can be altered by autoantibodies has changed the approach to the diagnosis and treatment of neuropsychiatric disorders previously considered idiopathic. Since 2007, seven such antibodies have been identified (anti-NMDAR, AMPAR, GABA(B), LGI1, Caspr2, GluR, and mGluR5), all targeting cell surface proteins involved in synaptic transmission, plasticity, or nerve excitability, and associated with syndromes that although severe, often respond to immunotherapy.1 Patients may be comatose for several months, with bizarre behaviors, abnormal movements, or refractory seizures and still recover with immunotherapy and extended care support.2 Considering that until recently these disorders were unknown, the relative high frequency of some has been surprising. For example, in a center focused in the diagnosis and epidemiology of encephalitis (California Encephalitis Project) the frequency of anti-NMDAR encephalitis surpassed that of any individual viral encephalitis.3 For these reasons, similar immune mechanisms are increasingly being considered in patients who develop rapidly progressive neuropsychiatric symptoms in the context of encephalitis of unknown etiology, a situation that occurs frequently. Nowadays about 70% of encephalitis of unclear etiology remain undiagnosed after extensive evaluation for infectious etiologies.4 In this setting, the identification of autoantibodies against neuronal cell surface antigens shifts the management to the use of immunotherapy and may extend the intensive care support in cases that otherwise might be considered futile.
In view of the above, the problem underlying the present invention resides in providing means for diagnosis and treatment of a previously unidentified autoimmune encephalitis, or encephalitis of unknown etiology, respectively.